Kuo C C, Wang S P, Grayston J T
Infect Immun. 1973 Jul;8(1):74-9. doi: 10.1128/iai.8.1.74-79.1973.
The infectivity of trachoma-inclusion conjunctivitis (TRIC) organisms (TW-5) was enhanced by pretreatment of HeLa cell monolayers before inoculation with diethylaminoethyl (DEAE)-dextran (30 mug/ml) and poly-l-lysine (10 mug/ml) and inhibited by dextran sulphate (250 mug/ml), fetuin (4%), ovomucoid (5%), N-acetyl neuraminic acid (0.5%), and Cholera vibrio neuraminidase (100 U/ml). The infectivity of lymphogranuloma venereum organisms (434) was not affected by DEAE-dextran, fetuin, and neuraminidase, was slightly inhibited by poly-l-lysine, and was inhibited by dextran-sulphate, ovomucoid, and N-acetyl neuraminic acid. The study suggested that sialic acid residues on the cell surface may be specific receptors for TRIC organisms. The receptors for TRIC organisms (TW-5 and TW-3) could be specifically blocked with inactivated (56 C for 30 min) TRIC organisms at the ratio of one live to 100 inactivated TRIC organisms, but not by inactivated lymphogranuloma venereum (434) or influenza virus (A(2)/Jap 305).
沙眼包涵体结膜炎(TRIC)病原体(TW - 5)的感染性,在接种前用二乙氨基乙基(DEAE)-葡聚糖(30微克/毫升)和聚 - L - 赖氨酸(10微克/毫升)预处理HeLa细胞单层后会增强,而被硫酸葡聚糖(250微克/毫升)、胎球蛋白(4%)、卵类粘蛋白(5%)、N - 乙酰神经氨酸(0.5%)和霍乱弧菌神经氨酸酶(100单位/毫升)抑制。性病性淋巴肉芽肿病原体(434)的感染性不受DEAE - 葡聚糖、胎球蛋白和神经氨酸酶影响,受聚 - L - 赖氨酸轻微抑制,被硫酸葡聚糖、卵类粘蛋白和N - 乙酰神经氨酸抑制。该研究表明细胞表面的唾液酸残基可能是TRIC病原体的特异性受体。TRIC病原体(TW - 5和TW - 3)的受体可用灭活的(56℃,30分钟)TRIC病原体以1个活的TRIC病原体比100个灭活的TRIC病原体的比例特异性阻断,但不能被灭活的性病性淋巴肉芽肿(434)或流感病毒(A(2)/Jap 305)阻断。